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• W2067312940 abstract "<i>Background:</i> The airway epithelial sodium channel (ENaC) is rate limiting for postnatal alveolar fluid clearance. Increased lung water content is a feature of respiratory distress syndrome (RDS), which is reduced by antenatal corticosteroid treatment in preterm infants. <i>Objectives:</i> Since corticosteroids also induce ENaC gene expression, we studied whether a repeat dose of antenatal β-methasone affects postnatal expression of airway ENaC. <i>Methods:</i> 17 pregnant women with imminent preterm birth were randomized to receive a single repeat dose of β-methasone (12 mg) or placebo (repeat β-methasone: 8 infants, gestational age (GA) 30.8 ± 2.2 weeks; placebo: 14 infants, GA 30.4 ± 2.7 weeks). Expression of α-, β- and γENaC subunits in nasal epithelium 1–5 and 20–29 h postnatally was analyzed with reverse transcription-PCR. <i>Results:</i> There were no differences between the study groups in RDS incidence or ENaC subunit expression (all p > 0.38). Regression coefficients for association of αENaC expression at 1–5 h with GA in infants with and without RDS differed significantly (p = 0.023). At 20–29 h, αENaC expression was lower in infants with RDS (p = 0.048). <i>Conclusions:</i> A single repeat dose of antenatal β-methasone did not increase ENaC expression, which may in part explain the absence of reduction in RDS incidence." @default.
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• W2067312940 date "2009-09-22" @default.
• W2067312940 modified "2023-09-26" @default.
• W2067312940 title "Expression of Airway Epithelial Sodium Channel in the Preterm Infant Is Related to Respiratory Distress Syndrome but Unaffected by Repeat Antenatal β-Methasone" @default.
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• W2067312940 doi "https://doi.org/10.1159/000239766" @default.
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